ArticleThe Journal of physiology2010
Activation of reverse Na+-Ca2+ exchange by the Na+ current augments the cardiac Ca2+ transient: evidence from NCX knockout mice.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 93 citations in OpenAlex.
- Cardiotoxicity Assessment of EGFR Tyrosine Kinase Inhibitors Using Human iPS Cell-Derived Cardiomyocytes and FDA Adverse Events Reporting System.Clinical and translational science · 2025Article
- Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Indoxyl Sulfate Induces Ventricular Arrhythmias Attenuated by Secretoneurin in Right Ventricular Outflow Tract Cardiomyocytes.Cardiovascular toxicology · 2025Article
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- T-type voltage-gated channels, NaCell communication and signaling : CCS · 2024Article
- NaV1.6 dysregulation within myocardial T-tubules by D96V calmodulin enhances proarrhythmic sodium and calcium mishandling.The Journal of clinical investigation · 2023Article
- Piezo1 is the cardiac mechanosensor that initiates the cardiomyocyte hypertrophic response to pressure overload in adult mice.Nature cardiovascular research · 2022Article
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Detrimental proarrhythmogenic interaction of CaNature communications · 2021Article
- Triiodothyronine maintains cardiac transverse-tubule structure and function.Journal of molecular and cellular cardiology · 2021Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- The NaFrontiers in pharmacology · 2021Article
- Na/Ca exchange in the atrium: Role in sinoatrial node pacemaking and excitation-contraction coupling.Cell calcium · 2020Review
- Berberine Mediated Positive Inotropic Effects on Rat HeartsFrontiers in pharmacology · 2020Article
- Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling.Antioxidants & redox signaling · 2019Article
- Tetrodotoxin-sensitive NaThe Journal of general physiology · 2018Article
- A privileged role for neuronal NaThe Journal of general physiology · 2018Article
- Optical Read-out of Neural Activity in Mammalian Peripheral Axons: Calcium Signaling at Nodes of Ranvier.Scientific reports · 2017Article
- Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.The Journal of physiology · 2017Review
- Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Current heart failure reports · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The hypothesis that Na(+) influx during the action potential (AP) activates reverse Na(+)-Ca(2+) exchange (NCX) and subsequent entry of trigger Ca(2+) is controversial. We tested this hypothesis by monitoring intracellular Ca(2+) before and after selective inactivation of I(Na) prior to a simulated action potential in patch-clamped ventricular myocytes isolated from adult wild-type (WT) and NCX knockout (KO) mice. First, we inactivated I(Na) using a ramp prepulse to 45 mV. In WT cells, inactivation of I(Na) decreased the Ca(2+) transient amplitude by 51.1 +/- 4.6% (P < 0.001, n = 14) and reduced its maximum release flux by 53.0 +/- 4.6% (P < 0.001, n = 14). There was no effect on diastolic Ca(2+). In striking contrast, Ca(2+) transients in NCX KO cardiomyocytes were unaffected by the presence or absence of I(Na) (n = 8). We obtained similar results when measuring trigger Ca(2+) influx in myocytes with depleted sarcoplasmic reticulum. In WT cells, inactivation of I(Na) decreased trigger Ca(2+) influx by 37.8 +/- 6% and maximum rate of flux by 30.6 +/- 7.7% at 2.5 mm external Ca(2+) (P < 0.001 and P < 0.05, n = 9). This effect was again absent in the KO cells (n = 8). Second, exposure to 10 mum tetrodotoxin to block I(Na) also reduced the Ca(2+) transients in WT myocytes but not in NCX KO myocytes. We conclude that I(Na) and reverse NCX modulate Ca(2+) release in murine WT cardiomyocytes by augmenting the pool of Ca(2+) that triggers ryanodine receptors. This is an important mechanism for regulation of Ca(2+) release and contractility in murine heart.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.